Uncoupling of eNOS, with increased generation of reactive oxygen species and impaired NO/cGMP signaling, was subsequently reported by the same group of investigators as an additional mechanism of the endothelial dysfunction elicited by chemerin in the rat aorta [9] and in human microvascular endothelial and smooth muscle cells via its chemokine-like receptor 1 (CMKLR1 or ChemR23) [35]. The gene discussed is CMKLR1; the disease is endothelial dysfunction.